Found programs: National Natural Science Foundation of China (No . 82002534) ; Research Project of Anhui Pro- vincial Institute of Translational Medicine (No . 2022zhyx-C71)
Authors:Ye Mengjie , Qu Weiwei , Luo Guangtao
Keywords:long non-coding RNA; LUCAT1 ; pancreatic cancer; MIA PaCa-2 ; tumor drug resistance; Akt
DOI:10.19405/j.cnki.issn1000-1492.2025.02.001
〔Abstract〕 Abstract Objective To investigate the effect of long non-coding RNA LUCAT1 (lncRNA LUCAT1) on the bio- logical behavior of MIA PaCa-2 in human pancreatic cancer cells , and to explore the potential role of LUCAT1 in the malignant progression of pancreatic cancer. Methods The mutation and expression of LUCAT1 in pancreatic cancer were analyzed by GEPIA , the expression levels of LUCAT1 in human pancreatic ductal cells HPNE and hu- man pancreatic cancer cells were detected by q-PCR , and the expression and distribution of LUCAT1 in human pancreatic cancer tissues were detected by FISH . CCK-8 assay and Transwell assay were used to detect the effects of LUCAT1 on the proliferation , apoptosis , drug resistance , and migration of MIA PaCa-2 cells . Gene ensemble enrichment analysis was performed to compare the related signaling pathways involved in LUCAT1 , and Western blot assay was used to verify the protein expression level . Results The results of GEPIA analysis showed that the expression level of LUCAT1 in human pancreatic cancer tissues was up-regulated , and the expression of LUCAT1 in human pancreatic cancer cells was significantly higher ( P < 0. 05) . Knockdown and overexpression of LUCAT1 could affect the proliferation , apoptosis , gemcitabine resistance , migration and invasion of pancreatic cancer cells , and the differences were statistically significant (P < 0. 05) . In addition , LUCAT1 affected p-Akt expression levels in pancreatic cancer and was inhibited after treatment with Akt inhibitor MK-2206 . Conclusion LUCAT1 regu- lates the malignant progression of MIA PaCa-2 in pancreatic cancer cells through the PI3K-Akt signaling pathway .